Any discussion of the prior art throughout the specification should in no way be considered as an admission that such prior art is widely known or forms part of the common general knowledge in the field.
Hypertension (high blood pressure) affects 26% of the adult population worldwide with an incidence of 30-33% in western countries. The world wide incidence of hypertension is expected to reach 29% by 2025 as a consequence of the westernisation of India and China. Current studies indicate that fewer than 20% of patients with hypertension attain their recommended blood pressure (BP) target and that to achieve these targets >75% of patients require therapy with multiple antihypertensive agents. Prehypertension (slightly elevated blood pressure) affects 31% of adults in the US and may develop into hypertension if not treated.
All currently available therapies have side effects:                Angiotensin Converting Enzyme Inhibitors (ACEI)—cough, angioneurotic oedema, hyperkalaemia;        Angiotensin Receptor Blockers (ARB's)—angioneurotic oedema, hyperkalaemia;        Calcium Channel Blockers (CCB)—flushing, leg/ankle oedema, constipation;        Thiazide diuretics—new onset diabetes, gout, hyponatraemia;        Beta (β) Blockers—new onset diabetes, inability to exercise, bradycardia, masking hypoglycaemia in diabetics; and        Aldosterone Antagonists—gynaecomastia, menorrhagia, hyperkalaemia.        
The need to use combination therapy increases the likelihood that patients will experience side effects and as a consequence not attain their BP target.
Hypertension and prehypertension are a major factor in the development of heart, kidney and blood vessel damage, resulting in the replacement of normal functional tissue by scar tissue or fibrosis. Some of the current antihypertensive agents—ACE inhibitors, ARB's renin inhibitors and aldosterone antagonists are able to slow the progression of the replacement of functional tissue by fibrosis, none have been shown to reverse existing fibrosis and restore normal tissue architecture. There is thus a need for agents which have to the efficacy to reduce BP significantly and thus enable a larger proportion of patients to attain BP target with single agent therapy and/or to reverse existing fibrosis and/or restore normal tissue architecture.
It is an object of the present invention to overcome or ameliorate at least one of the disadvantages of the prior art, or to provide a useful alternative.